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General Information
Symbol
Dmel\tslΔ
Species
D. melanogaster
Name
FlyBase ID
FBal0290718
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

Ends-out homologous recombination has resulted in the entire tsl coding region being replaced by a w marker. Deletion boundaries determined from primer sequences.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

The entire tsl coding region has been replaced by a w+mW.hs marker.

Insertion components
TI{TI}tslΔ
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Late embryos from tslΔ/tsl2 tslΔ/tsl3, tslΔ/tsl4, tslΔ/tsl5 transheterozygous and tslΔ homozygous mothers exhibit a fully penetrant "terminal class mutant" phenotype, in which some terminal structures are missing (including head structures, abdominal segment 8, telson, and filzkorper), as compared to controls; late embryos from tslΔ/tsl4, tslΔ/tsl5 transheterozygous and tslΔ homozygous mothers also exhibit an increasingly highly penetrant posterior-ventral cuticle hole phenotype, as compared to controls.

Gastrulating embryos from tslΔ homozygous mothers present an elongated, irregular and often incomplete ventral furrow, associated with delayed and patchy apical constriction, misaligned apical edges and apical mis-positioning of the nucleus in ventral domain cells, as compared to controls; these defects are more pronounced at the posterior region of the embryo, which frequently shows a complete failure in apical constriction. These gastrulating embryos also present failed posterior midgut invagination, leaving the pole cells and a large field of Twist-positive mesodermal tissue exposed at the dorsal surface, as compared to controls.

tslΔ mutant females are sterile, laying embryos that fail to specify terminal cell fate.

tslΔ mutant homozygotes show a significant delay of 26 hours to reach pupariation compared with heterozygous controls. The L2-L3 transition is delayed by ~7 hours. tslΔ mutant adult flies are 28% smaller than heterozygous controls and larvae are also noticeably smaller both at the wandering stage and throughout the third instar larval stage.

Wing cell density is significantly higher in tslΔ mutant flies compared with controls, indicating that cell size is reduced. Adult wings are also smaller than controls.

tslΔ/tsl5 mutant transheterozygotes are significantly delayed in reaching pupariation compared with controls.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference

tslΔ has abnormal size phenotype, non-suppressible by torrv66

Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

tslΔ is a suppressor of abnormal size phenotype of torrv66

NOT Suppressor of
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Suppressor of
NOT Suppressor of
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The ventral cuticle defects displayed by late embryos from tslΔ homozygous mothers are strongly enhanced by heterozygosity for RhoGEF24.4, leading to fully penetrant absence of ventral cuticle.

Late embryos from mothers both homozygous for tslΔ and expressing fogScer\UAS.P\T.cJa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 exhibit cuticle defects more similar to those of embryos from mothers only homozygous for tslΔ (i.e. some missing terminal structures and ventral-posterior cuticle hole) than those of embryos from mothers only expressing fogScer\UAS.P\T.cJa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 (i.e. only small amounts of recognizable cuticle remaining).

tslΔ torrv66 double mutants show a dramatically extended larval period compared to either mutant alone, with flies pupating 83 hours after controls. Double mutant adult flies are similar in size to tslΔ mutants alone.

A tslΔ mutant background does not suppress the advanced pupariation phenotype seen in flies expressing PtthScer\UAS.P\T.T:Ivir\HA1 under the control of Scer\GAL4phm.PO. The decrease in male body size is further enhanced. The embryonic patterning defects seen when PtthScer\UAS.P\T.T:Ivir\HA1 is expressed under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 are also not suppressed.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

The following defects exhibited by embryos from tslΔ mothers are partially rescued by one copy of tslT:Ivir\HA1 : the ventral cuticle hole, but not the "terminal class mutant" phenotype, in late embryos; both the irregularities/gaps in the ventral furrow and the exposure of mesodermal tissue (Twist-positive) at the dorsal surface, but not the elongated ventral furrow or the exposure of pole cells at the dorsal surface, in gastrulating embryos.

The expression of tslScer\UAS.T:Hsap\MYC,T:Avic\GFP-EGFP under the control of Scer\GAL4slbo.2.6 fully rescues the ventral cuticle hole and head defects, and partially rescues the patterning and cuticle defects exhibited by embryos from tslΔ mothers.

Expression of tslScer\UAS.cJa under the control of Scer\GAL4da-BG00643 rescues the delay in pupariation seen in tslΔ mutants. Expression of tslScer\UAS.cJa under the control of Scer\GAL4phm.PO is unable to rescue the phenotype.

Expression of tslT:Ivir\HA1 completely rescues the developmental delay and reduction in size seen in tslΔ mutant flies. The defect in terminal embryonic patterning is not rescued.

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Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (6)